Frequency of CCR5-Delta32 deletion in human immunodeficiency virus type 1 (HIV-1) in healthy blood donors, HIV-1-exposed seronegative and HIV-1-seropositive individuals of southern Brazilian population.
The frequency of CCR5-Delta32 allele in human immunodeficiency virus type 1 (HIV-1) infection in the southern Brazilian population was determined in a cross-sectional study carried out from October 2001 to June 2004. Genomic DNA was extracted from peripheral blood cells of 134 healthy blood donors, 145 HIV-1-exposed seronegative individuals, 152 HIV-1-seropositive asymptomatic individuals, and 478 HIV-1-seropositive individuals with AIDS. A fragment with 225 base-pairs of the CCR5 gene was amplified by polymerase chain reaction. The CCR5-Delta32 homozygous deletion was observed in 2 (1.5%) blood donors and in 1 (0.7%) individual HIV-1-exposed seronegative, and was absent among all the HIV-1-seropositive individuals (Fisher's exact test, p=0.0242). The frequency of the homozygous CCR5-Delta32 deletion in the HIV-1-exposed did not differ when compared with that observed in the HIV-1 seronegative blood donors (Fisher's exact test, p=0.6093; OR: 2.18, 95% CI: 0.11-129.6). The wild-type genotype CCR5/CCR5 frequency was higher among the HIV-1-seropositive with AIDS compared to HIV-1 seropositive asymptomatic individuals (Chi-square test, p=0.0263; OR: 2.02, 95% CI: 1.03-3.97). The absence of the homozygous deletion of CCR5-Delta32 among HIV-1-seropositive individuals underscored that this genotype is an important genetic factor associated with the decreased susceptibility to HIV-1 infection. The higher frequency of heterozygosity for the CCR5-Delta32 and the CCR5-Delta32 allele in HIV-1 seropositive asymptomatic compared to HIV-seropositive with AIDS individuals also underscored that this deletion could be associated with the delay of the HIV-1 disease progression in this population. However, the low frequency of CCR5-Delta32 homozygosity observed among HIV-1-exposed seronegative individuals shows that the allele could not explain, by itself, the natural resistance to HIV-1 infection and different mechanisms of protection against HIV-1 infection that must be involved in this population.
Reiche
Edna Maria Vissoci
EM
Health Sciences Center, Department of Pathology, Clinical Analysis and Toxicology, University Hospital of Londrina State University, Vila Operária, CEP 86.038-440, Londrina, Paraná, Brazil. reiche@sercomtel.com.br
Ehara Watanabe
Maria Angelica
MA
Bonametti
Ana Maria
AM
Morimoto
Helena Kaminami
HK
Akira Morimoto
Arilson
A
Wiechmann
Susana Lílian
SL
Matsuo
Tiemi
T
Carvalho De Oliveira
Jaqueline
J
Vissoci Reiche
Fernando
F
D000163:Acquired Immunodeficiency Syndrome / Q000235:genetics* / Q000276:immunology; D000483:Alleles; D001782:Blood Donors; D001938:Brazil; D005260:Female; D005787:Gene Frequency / Q000235:genetics / Q000276:immunology; D018023:HIV Seronegativity / Q000235:genetics*; D006679:HIV Seropositivity / Q000235:genetics* / Q000276:immunology; D015497:HIV-1 / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D008297:Male; D019713:Receptors, CCR5 / Q000235:genetics* / Q000276:immunology; D017384:Sequence Deletion
D019713:Receptors, CCR5